I. Direct Cardiac Compression
The concept of Direct Cardiac Compression (DCC) as a modality for circulation support comes from the emergent resuscitation of heart and lung. The most unique advantage of DCC, as compared to other existing Ventricular Assist Devices (VADs), lies in its non-blood contacting characteristic. By applying force directly to compress the decompressed heart, the extrinsic DCC devices help increase the ventricle contractile state and hereby improve the cardiac output. DCC can be fulfilled by, but not limited to, the following methods:
Skeletal Muscle Pump
This dynamic cardiomyoplasty method uses left latissimus dorsi muscle wrap to compress the decompensated heart. It takes time for muscle training and conversion, requiring patient condition be less emergent and have enough transition time for the muscle wrap to turn functional effective after surgery. Dynamic cardiomyoplasty met with difficulty in clinical trials and was terminated in the course of Phase III preparation due to insufficient patient recruitment. Major problems of muscle resistance to fatigue and the transformation of skeletal muscle into cardiac-like muscle were not satisfactorily resolved.
Mechanical Pumping Devices
This category comprises devices such as Anstadt Cup, CardioSupport System, Heart Booster, and HeartPatch, among others. Biocompatible material was used as the sac or cuff-like apparatus that deploys the externally applied compression forces. Fixation has been the major design concern of how the device is mounted onto the cardiac skin. Usually persistent suction power, glue adhesion or stay suture were used. Injurious complications include myocardial contusion, ischemia due to coronary artery compression, and frequent arrhythmias caused by asynchronous mechanical compression. To date, DCC devices can only be used in a short-term manner notwithstanding great effort has been tried to prolong the DCC usage period. HeartPatch DCC, however, uses separate, nonsurround patches placed on the ventricular free walls. The epicardial fusion adhesion was observed resulting from the tissue infusion of porous silicone material applied as the heart-contacting membrane. This fixation method avoids using persistent suction force and thus was intended for chronic use. All DCC devices showed effective enhancement in cardiac output. Nevertheless, the long-term efficacy has not been demonstrated and the complications that might arise due to improper fixation and epicardial actuation await further investigations.
Passive Mechanical Containment
This category of devices only provides restraining force to prevent further heart dilation. The avoidance of pathological enlargement of diseased heart was set as the design objective. Systolic enhancement has been critically limited by the small amount of elastic energy stored in the structural deformation of the sac in the diastolic phase. Acron Cardiac Support Device (CDS) is a representative apparatus. Acron CDS is an elastic textile net that wraps around both ventricles under the atrio-ventricular groove. It was found in chronic clinic trial that Acron net infused with the epicardium and thus caused myocardial fibrosis, leading to the impairment of cardiac contractility.
II. Cardiac Resynchronization Therapy
Cardiac resynchronization therapy (CRT) arises as a new and less traumatic treatment for congestive heart failure (CHF). About 30% CHF patients suffer dilated or ischemic cardiomyopathy, for which myocardial conduction delay manifests in the form of left bundle branch block and conduction heterogeneity have been the frequently observed symptoms. By way of electrical stimulation CRT can recoordinate contractile synchronization between left and right ventricles as well as among muscle segments within left ventricle (LV). Bi-ventricular and left ventricular pacing modes were found most effective in both acute studies and chronic CRT trials. Except for refractory advanced heart failure, conduction disordered patients who received CRT, in general, showed improvements in heart failure functional classification, quality of life and cardiac ejection fraction.
Acute hemodynamic improvements such as LV pressure gradient dp/dt increase, aortic pulse pressure elevation and averaged systolic pressure enhancement were observed upon acute ventricular pacing. A six-month chronic CRT trial tested on 25 patients indicates that left ventricle volume reduction occurred in a majority of patients with advanced heart failure. Similar large-scale random CRT test including 453 moderate-to-severe heart failure patients randomly divided into control and CRT groups also indicates benefits gained in hemodynamic performance and heart failure class function. Although studies in large patient cohorts with longer test periods are required to ascertain that CRT leads to cardiac reverse remodeling, the therapeutic outcome of reduced wall stress, myocardial oxygen consumption and mitral regurgitation already proved the general efficacy of CRT.
The pathologically enlarged cardiac chambers not only impair the myocardial contractility but also cause inhomogeneous inter- and intra-ventricular conduction delay, leading to inefficient use of muscle energy during cardiac contraction. Pacing with controlled atrioventricular conduction delay may reduce this asynchrony, literally at no expense of increased LV oxidative metabolism. Except for severely injured myocardium CRT can benefit some patients with elevated pulse pressure and intensity, manifested in terms of higher dp/dt in addition to gross symptom and ejection fraction improvements. The therapeutic rationale underlying this conduction recoordination is obvious. Myocardial contraction, which is the end point of electrical stimulation, could be resynchronized and hence functions in a more efficient manner to reduce the abnormal systolic workload and metabolic oxygen demand for the myocardium.
Electrophysiological alterations were frequently observed among advanced heart failure patients receiving chronic left ventricular assist device (LVAD) circulation support. It was reported that LVAD support resulted in immediate QRS interval decrease on the EKG waveform, indicating myocardial stress condition alteration. Moreover, QT interval, which reflects the repolarization of myocytes, shows an initial acute prolongation followed by a chronic shortening. Both QT prolongation and dispersion, and increased QRS duration are abnormal action potential characteristics associated with chronic heart failure. LVAD unloading, which immediately mitigates the pathological myocardial stretch due to excessive loading condition, may produce an acute inward current change across the ion channel, leading to the initial QT interval prolongation. Opposite myocardial repolarization behavior, however, appears in sustained cardiac unloading after weeks or months. It has been demonstrated in many LVAD unloaded patients that myocyte hypertrophy, ion homeostasis, cellular relaxation and adrenergic responsiveness were reversely remodeled. Although it is not clear whether those electrophysiological trend reversals were caused by shortened myocardium or by increased conduction velocity, mechanical unloading has consistently demonstrated its vital role in the reverse remodeling of LVAD-assisted failing hearts.